ArticleCirculation2019
Cronos Titin Is Expressed in Human Cardiomyocytes and Necessary for Normal Sarcomere Function.
Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- Nx3 Is a Z-Disk Structural and Signaling Hub That Is Reduced in Heart Failure.Circulation research · 2026Article
- Contractility Drives Cardiomyocyte Maturation and the Response to Nanopatterns.Circulation research · 2026Article
- Spatial relationships between vinculin tension and actin at cell adhesions define cell colony positioning and identity.Biophysical journal · 2026Article
- Pediatric dilated cardiomyopathy caused by TNNT2-R151W mutation: Modeling and rescue in patient-derived induced pluripotent stem cells and engineered heart tissue.Bioengineering & translational medicine · 2026Article
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- Location-Dependent Differences in Cardiac and Skeletal Muscle Dysfunction Associated With Truncating Titin (Circulation research · 2026Article
- Heterogeneity and optimal study design between cell lines in induced pluripotent stem cell-based cardiac disease modeling.Stem cells translational medicine · 2026Review
- TTN variants in pediatric cardiomyopathy: a retrospective cohort study.Frontiers in genetics · 2026Article
- Titin Cardiomyopathy, Emerging Evidence: More Than A Big Heart.Current cardiology reports · 2025Review
- Deregulated nutrient response in ttntv cardiomyopathy can be repaired via Erk inhibition for cardioprotective effects.Journal of molecular and cellular cardiology · 2025Article
- Regulation of TTN as a mechanism of and treatment for heart failure.The Journal of clinical investigation · 2025Article
- Dilated cardiomyopathy-associated skeletal muscle actin (ACTA1) mutation R256H disrupts actin structure and function and causes cardiomyocyte hypocontractility.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Proteolytic degradation of atrial sarcomere proteins underlies contractile defects in atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2024Article
- Loss of connectin novex-3 leads to heart dysfunction associated with impaired cardiomyocyte proliferation and abnormal nuclear mechanics.Scientific reports · 2024Article
- MBNL1 Regulates Programmed Postnatal Switching Between Regenerative and Differentiated Cardiac States.Circulation · 2024Article
- Allelic heterogeneity of TTNtv dilated cardiomyopathy can be modeled in adult zebrafish.JCI insight · 2024Article
- TTN truncation variants produce sarcomere-integrating proteins of uncertain functional significance.The Journal of clinical investigation · 2024Article
- Engineered Heart Tissues for Standard 96-Well Tissue Culture Plates.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Transcriptome studies of inherited dilated cardiomyopathies.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- Machine learning meets Monte Carlo methods for models of muscle's molecular machinery to classify mutations.The Journal of general physiology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 6 institutions in 5 countries.
Funding
Abstract
backgroundThe giant sarcomere protein titin is important in both heart health and disease. Mutations in the gene encoding for titin (
methodsTo investigate the function of titin in human CMs, we used CRISPR/Cas9 to generate homozygous truncations in the Z disk (TTN-Z
resultsAfter differentiation, we were surprised to find that despite the more upstream mutation, TTN-Z
conclusionsWe demonstrate that Cronos titin is expressed in developing human CMs and is able to support partial sarcomere formation in the absence of full-length titin. Furthermore, Cronos titin is necessary for proper sarcomere function in human induced pluripotent stem cell derived CMs. Additional investigation is necessary to understand the molecular mechanisms of this novel isoform and how it contributes to human cardiac disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.